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====Non-tPA Candidate====
 
====Non-tPA Candidate====
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#*If SBP >220 or DBP >120, lower by 25% over 24 hrs (drug of choice is Nicardipine)<ref>Zha AM, et al. Recommendations for management of large hemispheric infarction. Curr Opin Crit Care. 2015; 21(2):91-8.</ref>
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**If SBP >220 or DBP >120, lower by 25% over 24 hrs (drug of choice is Nicardipine)<ref>Zha AM, et al. Recommendations for management of large hemispheric infarction. Curr Opin Crit Care. 2015; 21(2):91-8.</ref>
#Aspirin 325mg (within 24-48hr)
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*Aspirin 325mg (within 24-48hr)
#Anticoagulation not recommended for acute stroke (even for A-fib)
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*Anticoagulation not recommended for acute stroke (even for A-fib)
  
 
====Endovascular Therapy====
 
====Endovascular Therapy====

Revision as of 16:57, 4 June 2015

Background

  • Vascular injury that reduces CBF to specific region of brain causing neuro impairment
  • Accurate determination of last known time when pt was at baseline is essential
Sensory Homonculus - courtesy AnatomyZone.com

Causes

  • Ischemic (87%)
    • Thrombotic (80% of ischemic CVA)
      • Atherosclerosis
      • Vasculitis
      • Arterial dissection
      • Polycythemia
      • Hypercoagulable state
      • Infection
    • Embolic (20% of ischemic CVA)
      • Valvular vegetations
      • Mural thrombi
      • Arterial-arterial emboli from proximal source
      • Fat emboli
      • Septic emboli
    • Hypoperfusion
      • Cardiac failure resulting in systemic hypotension
  • Hemorrhagic (13%)
    • Intracerebral
      • Hypertension
      • Amyloidosis
      • Anticoagulation
      • Vascular malformations
      • Cocaine use
    • SAH
      • Berry aneurysm rupture
      • Vascular malformation rupture

Clinical Presentation

Anterior Circulation

  • Blood supply via internal carotid system
  • Includes ACA and MCA

Internal Carotid Artery

  • Tonic gaze deviation towards lesion
  • Global aphasia, dysgraphia, dyslexia, dyscalculia, disorientation (dominant lesion)
  • Spatial or visual neglect (non-dominant lesion)

Anterior Cerebral Artery (ACA)

Signs and Symptoms:

  • Contralateral sensory and motor symptoms in the lower extremity (sparing hands/face)
  • Urinary and bowel incontinence
  • Left sided lesion: akinetic mutism, transcortical motor aphasia
  • Right sided lesion: Confusion, motor hemineglect
  • Presence of primitive grasp and suck reflexes
  • May manifest gait apraxia

Middle Cerebral Artery (MCA)

Signs and Symptoms:

  • Hemiparesis, facial plegia, sensory loss contralateral to affected cortex
  • Motor deficits found more commonly in face and upper extremity than lower extremity
  • Dominant hemisphere involved: aphasia
    • Wernicke's aphasia (receptive aphasia) -> patient unable to process sensory input and don't understand verbal communication
    • Broca's aphasia (expressive aphasia) -> patient unable to communicate verbally, even though understanding may be intact
  • Nondominant hemisphere involved: dysarthria (motor deficit of the mouth and speech muscles; understanding intact) w/o aphasia, inattention and neglect side opposite to infarct
  • Contralateral homonymous hemianopsia
  • Gaze preference toward side of infarct
  • Agnosia (inability to recognize previously known subjects)

Posterior circulation

Signs and Symptoms:

  • Crossed neuro deficits (i.e., ipsilateral CN deficits w/ contralateral motor weakness)
  • Multiple, simultaneous complaints are the rule (including loss of consciousness, nausea and vomiting, alexia, visual agnosia)
  • 5 Ds: Dizziness (Vertigo), Dysarthria, Dystaxia, Diplopia, Dysphagia
  • Isolated events are not attributable to vertebral occlusive disease (e.g. isolated lightheadedness, vertigo, transient ALOC, drop attacks)

Basilar artery

Signs and Symptoms:

  • Quadriplegia, coma, locked-in syndrome
  • "Crossed signs" in which a patient has unilateral cranial nerve deficits but contralateral hemiparesis and hemisensory loss suggest brainstem infarction
    • Millard-Gubler syndrome (ventral pontine syndrome) -- ipsilateral CN VI and VII palsy with contralateral hemiplegia of extremities
  • Sparing of vertical eye movements (CN III exits brainstem just above lesion)
    • Thus, may also have miosis b/l
  • One and a half syndrome (seen in a variety of brainstem infarctions)
    • "Half" - INO (internuclear opthalmoplegia) in one direction
    • "One" - inability for conjugate gaze in other direction
    • Convergence and vertical EOM intact
  • Medial inferior pontine syndrome (paramedian basilar artery branch)
    • Ipsilateral conjugate gaze towards lesion (PPRF), nystagmus (CN VIII), ataxia, diplopia on lateral gaze (CN VI)
    • Contralateral face/arm/leg paralysis and decreased proprioception
  • Medial midpontine syndrome (paramedian midbasilar artery branch)
    • Ipsilateral ataxia
    • Contralateral face/arm/leg paralysis and decreased proprioception
  • Medial superior pontine syndrome (paramedian upper basilar artery branches)
    • Ipsilateral ataxia, INO, myoclonus of pharynx/vocal cords/face
    • Contralateral face/arm/leg paralysis and decreased proprioception

Superior Cerebellar Artery (SCA)

  • ~2% of all cerebral infarctions[1]
  • May present with nonspecific symptoms - N/V, dizziness, ataxia, nystagmus (more commonly horizontal)[2]
  • Lateral superior pontine syndrome
    • Ipsilateral ataxia, n/v, nystagmus, Horner's syndrome, conjugate gaze paresis
    • Contralateral loss of pain/temperature in face/extremities/trunk, and loss of proprioception/vibration in LE > UE

Posterior Cerebral Artery (PCA)

Signs and Symptoms:

  • Common after CPR, as occiptal cortex is a watershed area
  • Unilateral headache (most common presenting complaint)
  • Visual field defects (contralateral homonymous hemianopsia, unilateral blindness)
  • Visual agnosia - can't recognize objects
  • Possible macular sparing if MCA unaffected
  • Motor function is typically minimally affected
  • Lateral midbrain syndrome (penetrating arteries from PCA)
    • Ipsilateral CN III - eye down and out, pupil dilated
    • Contralateral hemiataxia, tremor, hyperkinesis (red nucleus)
  • Medial midbrain syndrome (upper basilar and proximal PCA)
    • Ipsilateral CN III - eye down and out, pupil dilated
    • Contralateral paralysis of face, arm, leg (corticospinal)

Anterior Inferior Cerebellar Artery (AICA)

  • Lateral inferior pontine syndrome
  • Ipsilateral facial paralysis, loss of corneal reflex (CN VII)
  • Ipsilateral loss of pain/temp (CN V)
  • Nystagmus, N/V, vertigo, ipsilateral hearing loss (CN VIII)
  • Ipsilateral limb and gait ataxia
  • Ipsilateral Horner syndrome
  • Contralateral loss of pain/temp in trunk and extremities (lateral spinothalamic)

Posterior Inferior Cerebellar Artery (PICA)

Signs and Symptoms:

  • Lateral medullary/Wallenberg syndrome
  • Ipsilateral cerebellar signs, ipsilateral loss of pain/temp of face, ipsilateral Horner's syndrome, ipsilateral dysphagia and hoarseness, dysarthria, vertigo/nystagmus
  • Contralateral loss of pain/temp over body
  • Also caused by vertebral artery occlusion (most cases)

Internal Capsule and Lacunar Infarcts

  • May present with either lacunar c/l pure motor or c/l pure sensory (of face and body)[3]
    • Pure c/l motor - posterior limb of internal capsule infarct
    • Pure c/l sensory - thalamic infarct (Dejerine and Roussy syndrome)
  • C/l motor plus sensory if large enough
  • Clinically to cortical large ACA + MCA stroke - the following signs suggest cortical rather than internal capsule[4]:
    • Gaze preference
    • Visual field defects
    • Aphasia (dominant lesion, MCA)
    • Spatial neglect (non-dominant lesion)
  • Others
    • I/l ataxic hemiparesis, with legs worse than arms - posterior limb of internal capsule infarct
    • Dysarthria/Clumsy Hand Syndrome - basilar pons or anterior limb of internal capsule infarct

Anterior Spinal Artery (ASA)

Superior ASA

  • Medial medullary syndrome - displays alternating pattern of sidedness of symptoms below
  • Contralateral arm/leg weakness and proprioception/vibration
  • Tongue deviation towards lesion

Inferior ASA

  • ASA syndrome
  • Watershed area of hypoperfusion in T4-T8
  • B/l pain/temp loss in trunk and extremities (spinothalamic)
  • B/l weakness in trunk and extremities (corticospinal)
  • Preservation of dorsal columns

Differential Diagnosis

Weakness

Diagnosis

Work-Up

  1. Bedside glucose
  2. Bedside Hb (polycythemia)
  3. CBC
  4. Chemistry
  5. Coags
  6. Troponin
  7. ECG (esp A-fib)
  8. Head CT
    • Primarily used to exclude intracranial bleeding, abscess, tumor, other stroke mimics
  9. Also consider:
    • Pregnancy test
    • CXR (if infection suspected)
    • UA (if infection suspected)
    • Utox (if ingestion suspected)

Management

Ischemic

Both tPA AND non-tPA candidates

  • Prevent dehydration
  • Maintain SpO2 >92%
  • Maintain blood glucose between 140 and 180 mg/dL
  • Prevent fever
  • HOB >30°

tPA Candidate

  1. tPA
  2. Hypertension
    • Lower SBP to <185, DBP to <110
    • Options:
      1. Labetalol 10–20mg IV over 1–2 min; may repeat x1 OR
      2. Nitroglycerin paste, 1–2 in. to skin OR
      3. Nicardipine 5mg/hr, titrate up by 2.5mg/hr at 5-15min intervals; max dose 15mg/hr
        • When desired blood pressure attained reduce to 3mg/hr

Non-tPA Candidate

  • Hypertension
    • Allow permissive HTN
    • If SBP >220 or DBP >120, lower by 25% over 24 hrs (drug of choice is Nicardipine)[5]
  • Aspirin 325mg (within 24-48hr)
  • Anticoagulation not recommended for acute stroke (even for A-fib)

Endovascular Therapy

  • Therapy includes endovascular tPA administration or mechanical clot removal
  • Early trials MR RESCUE, SYNTHESIS, and IMSIII showed no benefit and potential harm
  • MR CLEAN Trial show promising outcomes[6]
    • Participants had proximal intracranial artery occlusions
    • Intervention was conducted within 6 hrs
    • Functional independence of 32.6% with endovascular treatment and 19.1% with typical therapy

Hemorrhagic

Cerebellar

  • Early neurosurgical consultation is needed (herniation may lead to rapid deterioration)
  • See Cerebellar Stroke

See Also

External Links

References

  1. Macdonell RA, Kalnins RM, Donnan GA. Cerebellar infarction: natural history, prognosis, and pathology. Stroke. 18 (5): 849-55.
  2. Lee H, Kim HA. Nystagmus in SCA territory cerebellar infarction: pattern and a possible mechanism. J Neurol Neurosurg Psychiatry. 2013 Apr;84(4):446-51.
  3. Rezaee A and Jones J et al. Lacunar stroke syndrome. Radiopaedia. http://radiopaedia.org/articles/lacunar-stroke-syndrome.
  4. Internal Capsule Stroke. Stanford Medicine Guide. http://stanfordmedicine25.stanford.edu/the25/ics.html
  5. Zha AM, et al. Recommendations for management of large hemispheric infarction. Curr Opin Crit Care. 2015; 21(2):91-8.
  6. Berkhemer OA, et al. A randomized trial of intraarterial treatment for acute ischemic stroke. NEJM. 2015; 372(1):11-20.